Atrium (heart)

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Atrium
Diagram of the human heart (cropped).svg
Front view of heart showing the atria
Identifiers
Gray's p.528
TA A12.1.00.017
FMA FMA:7099
Anatomical terminology

The atrium (plural: atria) is one of the two blood collection chambers of the heart. It was previously called the auricle, but that name has now been in use as being synonymous with the right or left atrial appendage.[1] The atrium is a chamber in which blood enters the heart, as opposed to the ventricle, where it is pushed out of the organ. It has a thin-walled structure that allows blood to return to the heart. There is at least one atrium in animals with a closed circulatory system.

The atrium receives blood as it returns to the heart to complete a circulating cycle, whereas the ventricle pumps blood out of the heart to start a new cycle.[2][3]

Structure[edit]

Main articles: Left atrium and Right atrium

Humans have a four-chambered heart consisting of the right atrium, left atrium, right ventricle, and left ventricle. The atria, are the two upper chambers. The right atrium receives and holds deoxygenated blood from the superior vena cava, inferior vena cava and coronary sinus, which it then sends down to the right ventricle which in turn sends it to the pulmonary trunk and artery for pulmonary circulation. The left atrium receives the oxygenated blood from the left and right pulmonary veins, which it pumps to the left ventricle for pumping out through the aorta for systemic circulation.[4][5]The atria do not have valves at their inlets.[6] As a result, a venous pulsation is normal and can be detected in the jugular vein as the jugular venous pressure.[7][8] Internally, there are the rough pectinate muscles and crista terminalis of His, which act as a boundary inside the atrium and the smooth walled part derived from the sinus venosus.[9]The interatrial septum separates the right atrium from the left atrium and this is marked by a fossa ovalis which is used in the fetal period as a means of bypassing the lung. The atria are depolarised by calcium.

Nodes[edit]

The sinoatrial (SA) node is located in the right atrium, next to the superior vena cava. This is a group of pacemaker cells which spontaneously depolarize to create an action potential. The cardiac action potential then spreads across both atria causing them to contract, forcing the blood they hold into their corresponding ventricles.

Development[edit]

During embryogenesis at about two weeks, a primitive atrium begins to be formed. It begins as one chamber which over the following two weeks becomes divided by the septum primum into the left atrium and the right atrium. The interatrial septum in the right atrium has an opening, the foramen ovale which provides access to the left atrium; this connects the two chambers, which is essential for fetal blood circulation. At birth, when the first breath is taken fetal blood flow is reversed to travel through the lungs. The foramen ovale is no longer needed and it closes to leave a depression (the fossa ovalis) in the atrial wall.

In some cases, the foramen ovale fails to close and is present in 20% of the general population; This is known as a patent foramen ovale, an atrial septal defect. However, it is mostly unproblematic.

Within the fetal right atrium, blood from the inferior vena cava and the superior vena cava flow in separate streams to different locations in the heart, and this has been reported to occur through the Coandă effect.[10]

Function[edit]

In human physiology, the atria facilitate circulation primarily by allowing uninterrupted venous flow to the heart during ventricular systole.[11][12] By being partially empty and distensible, atria prevent the interruption of venous flow to the heart that would occur during ventricular systole if the veins ended at the inlet valves of the heart. In normal physiologic states, the output of the heart is pulsatile, and the venous inflow to the heart is continuous and non-pulsatile. But without functioning atria, venous flow becomes pulsatile, and the overall circulation rate decreases significantly.[13][14]

Atria have four essential characteristics that cause them to promote continuous venous flow. (1) There are no atrial inlet valves to interrupt blood flow during atrial systole. (2) The atrial systole contractions are incomplete and thus do not contract to the extent that would block flow from the veins through the atria into the ventricles. During atrial systole, blood not only empties from the atria to the ventricles, but blood continues to flow uninterrupted from the veins right through the atria into the ventricles. (3) The atrial contractions must be gentle enough so that the force of contraction does not exert significant back pressure that would impede venous flow. (4) The "let go" of the atria must be timed so that they relax before the start of ventricular contraction, to be able to accept venous flow without interruption.[15][16]

By preventing the inertia of interrupted venous flow that would otherwise occur at each ventricular systole, atria allow approximately 75% more cardiac output than would otherwise occur. The fact that atrial contraction is 15% of the amount of the succeeding ventricular ejection has led to a misplaced emphasis on their role in pumping up the ventricles (the so-called "atrial kick"), whereas the key benefit of atria is in preventing circulatory inertia and allowing uninterrupted venous flow to the heart.[17][18]

Also, of importance in maintaining the blood flow are the presence of atrial volume receptors. These are low-pressure baroreceptors in the atria, which send signals to the hypothalamus when a drop in atrial pressure (which indicates a drop in blood volume) is detected. This triggers a release of vasopressin.[19]

Clinical significance[edit]

Other animals[edit]

In fish, the circulatory system is very simple: a two-chambered heart including one atrium and one ventricle. In other vertebrate groups, the circulatory system is much more complicated. Their circulatory systems are divided into two types: a three-chambered heart, with two atria and one ventricle, or a four-chambered heart, with two atria and two ventricles.

See also[edit]

This article uses anatomical terminology; for an overview, see anatomical terminology.

References[edit]

  1. ^ http://www.drugs.com/dict/auricles-of-atria.html
  2. ^ http://www.healthsystem.virginia.edu/uvahealth/adult_cardiac/anatomy.cfm
  3. ^ http://www.ivy-rose.co.uk/HumanBody/Blood/Heart_Structure.php
  4. ^ http://www.ivy-rose.co.uk/HumanBody/Blood/Heart_Structure.php
  5. ^ Human heart anatomy diagram. Retrieved on 2010-07-02.
  6. ^ http://www.americanheart.org/presenter.jhtml?identifier=4598
  7. ^ http://www.patient.co.uk/doctor/Jugular-Venous-Pressure.htm
  8. ^ http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A622#A629
  9. ^ http://www.med.unc.edu/embryo_images/unit-cardev/cardev_htms/cardev040.htm
  10. ^ Ashrafian H. The Coanda effect and preferential right atrial streaming. Chest. 2006 Jul;130(1):300.
  11. ^ Anderson, RM. The Gross Physiology of the Cardiovascular System (2nd ed., 2012). See "Chapter 1: Normal Physiology."
  12. ^ Anderson, R.M., Fritz, J.M., and O’Hare, J.E. “The Mechanical Nature of the Heart as a Pump.” American Heart Journal 73 (1967): 92-105.
  13. ^ The Determinants of Cardiac Output (video produced by University of Arizona Biomedical Communications; demonstration of atrial effect begings at 13:43).
  14. ^ http://cardiac-output.info (See discussion of atrial effect in text Chapter 1.)
  15. ^ Anderson, RM. The Gross Physiology of the Cardiovascular System (2nd ed.) See "Chapter 1: Normal Physiology."
  16. ^ Anderson, R.M., Fritz, J.M., and O’Hare, J.E. “The Mechanical Nature of the Heart as a Pump.” American Heart Journal 73 (1967): 92-105.
  17. ^ The Gross Physiology of the Cardiovascular System at 11.
  18. ^ Anderson, R.M., Fritz, J.M., and O’Hare, J.E. “The Mechanical Nature of the Heart as a Pump.” American Heart Journal 73 (1967): 92-105.
  19. ^ Sherwood, Lauralee (2008). Human physiology: From cells to systems (7th revised ed.). Cengage Learning. p. 567. ISBN 978-0-495-39184-5.